Oxidative stress and mitochondrial impairment are major players in ME/CFS, which is why there is so much overlap between the symptoms of GWI and ME/CFS. This is also why CoQ10 has been a staple in ME/CFS treatment arsenal since the late 1980s, when the Behans noted damage to the mitochondria in muscle tissues of ME patients in the UK._____________________________________

Coenzyme Q10 Helps Veterans Battle Gulf War Illness Symptoms

Press Release: UC San Diego, November 3, 2014. Roughly one-third of the 700,000 United States troops who fought in the 1990-1991 Persian Gulf War have subsequently developed a distinct set of chronic health problems, dubbed Gulf War illness. Their symptoms, from fatigue, muscle pain and weakness to decreased cognitive function and gastrointestinal and skin problems, persist decades after the conflict.

In a study published in the Nov. 1 issue of Neural Computation, researchers at the University of California, San Diego School of Medicine report that a high quality brand of coenzyme Q10 (CoQ10) – a compound commonly sold as a dietary supplement – provides health benefits to persons suffering from Gulf War illness symptoms.

Forty-six United States Gulf War veterans participated in the randomized, double-blind, placebo-controlled study. Each veteran had been diagnosed with Gulf War illness.

“Gulf War illness is not the same as post-traumatic stress disorder or traumatic brain injury, signature illnesses of later deployments, which are caused by psychological and mechanical injury, respectively,” said Beatrice Golomb, MD, PhD, professor of medicine at UC San Diego School of Medicine and principal investigator on the study. “Evidence instead links Gulf War illness to chemical exposures, such as pesticides or pills given to soldiers to protect them from possible nerve agents. These chemicals can damage mitochondria, which generate the energy our cells need to do their jobs. When these powerhouses of the cells are disrupted, it can produce symptoms compatible with those seen in Gulf War illness.”

The connection to chemical and toxin exposures is fortified by evidence of mitochondrial problems in affected veterans, said Golomb, as well as evidence showing those veterans who became ill are significantly more likely than others to harbor genetic variants that render their enzymes less effective at detoxifying these chemicals.

CoQ10 is a fat-soluble antioxidant made by the body to support basic cell functions, including directly assisting mitochondrial energy production. Over a course of three and a half months, the veterans in the study received a pill form of either CoQ10 or a placebo. Researchers found 80 percent of those who received 100mg of CoQ10 had improvement in physical function. The degree of improvement correlated to the degree in which CoQ10 levels in the blood increased.

The researchers reported that Gulf War illness symptoms like headaches, fatigue with exertion, irritability, recall problems and muscle pain also improved.

“The statistical significance of these benefits, despite the small sample size, underscores the large magnitude of the effects,” Golomb said. “Mounting evidence suggests findings in Gulf War illness are relevant to toxin-induced health problems in the civilian sector, so what we learn by studying health challenges of these veterans, will likely benefit others.”

Golomb and colleagues are seeking additional funding to test a more complete “mitochondrial cocktail,” which combines CoQ10 with additional nutrients that support cell energy and reduce oxidative damage to cells.

Recently, a group of researchers at UC Davis discovered that HIV evades detection, and eradication, by hiding in the gut.

They also discovered how.The mechanism is simple. First the gut responds to the virus by activating immune cells that release the pro-inflammatory cytokine, IL-beta. IL-beta breaks down the lining of the gut, causing leaky gut. The viruses then spread throughout the system.

Although this research focuses on HIV, it has profound implications for the mechanism - and treatment - of ME/CFS. Dr. Chia has proposed that enteroviruses, which reside in the intestines, are involved in the etiology of ME/CFS. He found that 82% of the patients he tested showed persistent enteroviral infections in the gut. Dr. John Richardson, a British physician (now deceased) who treated thousands of patients with ME/CFS, noted that 20% of his patients developed ME/CFS after enteroviral infections (Coxsackie virus).

Interestingly, while both Dr. Myhill and Dr. Cheney have maintained that leaky gut is a major problem in ME/CFS, both have attributed the loss of structural integrity of the gut lining to mitochondrial dysfunction. Given the presence of elevated pro-inflammatory cytokines - such as interleukin-1 beta - in patients with ME/CFS (Cannon et al. 1996, Maes et al, 2012), the persistent flu-like symptoms and immune up-regulation found in many ME/CFS patients might be more elegantly explained by the mechanism outlined below.

One important benefit of this research is that it opens the door to treatment. The authors of the study have proposed a fairly simple solution to the problem of leaky gut. Lactobacillus plantarum is a probiotic that blocks IL-beta. It is also fairly inexpensive, readily available, and does not require a prescription.What is remarkable about this research is that for decades complementary and alternative physicians have blamed food intolerance on leaky gut. Yet most mainstream physicians deny its very existence, because the diagnosis is not taught in medical school. I was told just last week by a gastroenterologist that "leaky gut" was a hypothetical ailment that could not be tested for or treated.

It appears he was wrong.__________________________

Surprising discovery: HIV hides in gut, evading eradication

Inflammatory response breaks down intestinal lining, but help may come from friendly bacteria

Press Release: UC Davis Health System. (SACRAMENTO, Calif.) — Researchers at UC Davis have made some surprising discoveries about the body's initial responses to HIV infection. Studying simian immunodeficiency virus (SIV), the team found that specialized cells in the intestine called Paneth cells are early responders to viral invasion and are the source of gut inflammation by producing a cytokine called interleukin-1 beta (IL-1β).

Though aimed at the presence of virus, IL-1β causes breakdown of the gut epithelium that provides a barrier to protect the body against pathogens. Importantly, this occurs prior to the wide spread viral infection and immune cell killing. But in an interesting twist, a beneficial bacterium, Lactobacillus plantarum, helps mitigate the virus-induced inflammatory response and protects gut epithelial barrier. The study was published in the journal PLoS Pathogens.

One of the biggest obstacles to complete viral eradication and immune recovery is the stable HIV reservoir in the gut. There is very little information about the early viral invasion and the establishment of the gut reservoir.

"We want to understand what enables the virus to invade the gut, cause inflammation and kill the immune cells," said Satya Dandekar, lead author of the study and chair of the Department of Medical Microbiology and Immunology at UC Davis.

"Our study has identified Paneth cells as initial virus sensors in the gut that may induce early gut inflammation, cause tissue damage and help spread the viral infection. Our findings provide potential targets and new biomarkers for intervening or blocking early spread of viral infection," she said.

In the study, the researchers detected a very small number of SIV infected cells in the gut within initial 2.5 days of viral infection; however, the inflammatory response to the virus was playing havoc with the gut lining. IL-1β was reducing the production of tight-junction proteins, which are crucial to making the intestinal barrier impermeable to pathogens. As a result, the normally cohesive barrier was breaking down.

Digging deeper, the researchers found the inflammatory response through IL-1β production was initiated in Paneth cells, which are known to protect the intestinal stem cells to replenish the epithelial lining. This is the first report of Paneth cell sensing of SIV infection and IL-1β production that links to gut epithelial damage during early viral invasion. In turn, the epithelial breakdown underscores that there's more to the immune response than immune cells.

"The epithelium is more than a physical barrier," said first author Lauren Hirao. "It's providing support to immune cells in their defense against viruses and bacteria."

The researchers found that addition of a specific probiotic strain, Lactobacillus plantarum, to the gut reversed the damage by rapidly reducing IL-1β, resolving inflammation, and accelerating repair within hours. The study points to interesting possibilities of harnessing synergistic host-microbe interactions to intervene early viral spread and gut inflammation and to mitigate intestinal complications associated with HIV infection.

"Understanding the players in the immune response will be important to develop new therapies," said Hirao. "Seeing how these events play out can help us find the most opportune moments to intervene."

Dr. Jay Streastrunk (now deceased) was a pediatric and adolescent psychiatrist who had a clinical practice in Texas and California. He was known for his explanation of the primary mechanism of multiple chemical sensitivities - "kindling" - and for his willingness to treat patients with an illness that most doctors still don't believe is "real."Kindling is a neurological mechanism through which repeated exposures to a stimulus can sensitize an individual so that even a small stimulus produces a reaction. In neurological circles, kindling has been linked to seizures. Among allergists, kindling is known as "sensitization." It accounts for why even a hint of peanut can cause anaphylactic shock in an allergic individual. Kindling also is involved in FM and other pain syndromes.

In 2009, Jason et al. proposed that kindling was part of the etiology of ME/CFS. In a paper titled, "Kindling and Oxidative Stress as Contributors to Myalgic Encephalomyelitis/Chronic Fatigue Syndrome", the authors state:"Viral exposure early in life could trigger an immunologic cascade with significant effects on kindling. The release of TNF-alpha and other mediators could contribute to immunologic sensitization through inflammation and corticosteroid mediation. This then might leave an individual primed to respond in an adverse fashion to a future stressor event through amygdala and hippocampal kindling. The response to a stressor event then might reintroduce an inflammatory response that could contribute to the development of lesions and symptomatology. This could help explain why viral exposure does not necessarily trigger immediate symptomatology."This model is in keeping with the theory of occult infection - an infection which remains latent, or asymptomatic, until a second stressor is introduced. However, Jason et al. took the model one step further by proposing that the repetition of the exposure over time leads not only to an increasingly sensitive nervous system (which is why relapses often manifest differently from the initial illness), but to a prolonged inflammatory cycle.

Below is Dr. Seastrunk's excellent explanation of kindling. The treatment he recommended for kindling was Neurontin (gabapentin), a neuro-inhibitory drug also favored by Dr. Jay Goldstein. Some ME/CFS patients have reported benefits from gabapentin, however, as with all treatments, responses to gabapentin are mixed._____________________________________________________

KINDLING , FOCAL BRAIN INJURY AND CHEMICAL and ELECTRICAL SENSITIVITY in the production of "Environmental Disease"

by Jay Seastrunk

Kindling

In the 1960's while doing research at Tulane Medical School, I became interested in the correlation between the electrical manifestation of brain activity and behavior. I was fortunate enough to be able to participate in deep electrode long term implant studies in non-psychotic and psychotic individuals. This experience strongly imprinted in me the connection between brain activity and behavior. In reviewing the literature for Dr. R. G. Heath, my department chairman, I came across the "mirror focus" literature.

In 1949, Pope et.al., described the "mirror focus" phenomenon, while working with Penfield on man and monkeys. In "mirror focus" development, an epileptic focus (a mirror focus) is found to develop in the hemisphere opposite to an original epileptic focus, even though there has never been an injury in that hemisphere. This developed focus takes ten to fifteen years to emerge in humans. In 1969, Goddard and two other researchers in the field of epilepsy published an article entitled, "A Permanent Change in Brain Function Resulting from Daily Electrical Stimulation". They were curious as to why an incubation period often elapsed between a traumatic brain injury, and the occurrence of a first seizure, months to years after the injury.

What they discovered was that repeated applications of either chemical or electrical irritants to the brains of animals eventually produce intense seizure discharges, even if each one of the irritating stimulation themselves is incapable of producing a seizure. They discovered that a stimulus to the brain, that ordinarily would produce no change in either the animal's behavior or in the electrical activity of its brain, did produce significant changes in both behavior and electrical activity, if it were repeated and repeated. They called the repeated stimulus "a chronic irritant", and the resulting effect "kindling." In Vietnam veterans, psychosis took fifteen years to emerge following brain injury illustrating that the limbic and/or more subtle behavioral manifestations of brain injury take a long time to emerge perhaps related to the "kindling" phenomena.

In 1992, Bell and her co-workers applied this reasoning to chemical sensitivity. They pointed out that the olfactory system of animals and humans permits access (via the nose) of environmental chemicals directly into the brain. These molecules pass into the entry point of the smell system, called the olfactory bulb. Numerous projections from this part of the brain are present in the upper regions of the nose and permit aromas, perfumes, aromatic hydrocarbons, and solvents to pass into the brain. Even more remarkable than the fact that these molecules pass directly into the brain, is the fact that they can progress neuron by neuron to the furthest reaches of the emotional portion of the brain, called the limbic system.

The limbic system, located primarily in the temporal lobe, serves not only as the location of our emotions, but even more interestingly, it is the location where we organize our information into understandable categories. This is because in animals, smeil has great significance. An odor can mean the difference between food or poison, and friend or foe, so it is reasonable that odors and their significance would be closely linked in the animal brain.

The limbic system, located partially in the temporal lobe, serves, not only as the location of our emotional system, but even more interestingly, as an information organizer, where we process information into understandable perceptions, wheather they are olfactory, visual, tactile, or auditory. Memory with its emotional conections is stored here However, it is tuned into many more inputs than just a single sensory perception. In fact, it seems to be tuned into all possible inputs, whether sensory, imaginative, verbal, or motor. This is why odors, movements, sights, sounds, ideas, or a combination of these can rapidly trigger memories, emotions, and behaviors.

When the limbic temporal lobe is injured, the individual cannot always recall memories at will, even though the memory is still in the brain. Individuals affected with chemical injuries frequently report that they are having memory problems, yet are surprised when psychological tests show no memory damage. This is because the system where the memories are stored, which is analogous to the bookshelves in a library is intact; it is the memory organization and retrieval system or the card catalogue of the library that has been injured.

How does the kindling and the mirror focus phenomenon fit into this? Researchers into epilepsy have long known that the olfactory and limbic systems are particularly susceptible to kindling. In fact, two limbic structures, the amygdala and the hippocampus are frequently used in animals to study epilepsy, because of the ease with which they can be kindled.

This means that individuals whose brains have been injured can be kindled by either repeated low level stimulation of a chemical or electrical irritant, or by a single peak exposure. Thus, an individual will continue to experience more and more effects from exposures too weak to affect a previously unaffected person and possibly become more and more sensitive to weaker and weaker exposures.

Time-Dependent Sensitization

A second mechanism, called time-dependent sensitization, is almost identical to kindling. According to Bell et al. (1992), time-dependent sensitization is very similar to kindling in that an external substance, e.g. a chemical, that has no effect at first on an animal's brain will later produce a major reaction. This sounds almost like kindling, except for a few minor differences. By definition, kindling eventually leads to seizures, whereas time-dependent sensitization does not necessarily lead to seizures. Instead, it can lead to changes in the animal's behavior, its sensations, cognitions, autonomic nervous system responses, vestibuiar (balance) responses, motion responses, and/or or in hs immune or hormonal function.

Another difference is that time-dependent sensitization can occur after a single intense exposure, rather than a few small, repeated ones. After the passage of time, and without further exposure, a new exposure will suddenly produce the altered experience and/or behavior, or alter the immune function.

Finally, time-dependent sensitization shows cross-sensitization, which means that after a given individual is sensitized, other substances, different from the one causing the initial exposure, will now produce the altered experience, and/or behavior or function in a stereotyped way for each individual.

Kindling and time-dependent sensitization answer one of the most mysterious aspects of chemical and electrical sensitivity i.e. who gets affected and why? Another phenomenon, known as cacosmia, must be introduced to understand this

RISK FACTORS FOR CHEMICAL NEUROTOXICITY

On November 13, 1993, over 400 affected workers, health care professionals, and interested labor and management representatives listened to Dr. Bell present her latest findings to a conference hosted by the Washington Toxics Coalition in Seattle, WA. What she and her co-workers suggested is that there is an identifiable group of people more at risk for the development of chemical brain injury than other more resistant individuals.

To be able to identify these individuals, it is first necessary to understand a new term. The new term is cacosmia (ca-COS'-mi-a), which means "an altered sense of smell, accompanied by a tendency to feel ill i.e. nausea, headache, and dizziness from the odor of chemicals at low levels (that have no effect on normals." In other words, cacosmic individuals are the ones who first notice and are affected by the chemical odors in an environment. Six per cent of college students report cacosmia when asked if they develop illness when exposed to pesticides, car exhaust, paint, perfumes, or new carpet. Among the individuals that were studied, women represented 79% of those identified as the most cacosmic.

Among both women and men who were identified as strongly cacosmic, there was a much higher incidence of reported food allergies, self-reported memory loss, and somatic symptoms in general, when compared with noncacosmic subjects.

For electromagnetically sensitive patients, a similar recruitment, sometimes by subliminal visual, or auditory inputs, or by electromagnetic waves themselves, activate a kindled brain focus, causing it to fire, producing the characteristic, stereotyped, repetitive symptoms of that individual's "reaction".

A second risk factor appears to be stress. Ester Stemberg described how the central nervous system affects the immune system through endocrine, paracrine, and neuronal mechanisms. Bell, also, points out that one of the stress hormones in the brain, CRH, cannot only itself produce kindling, but when present in above normal amounts, makes it more likely that other external stimuli will induce kindling. Stress and sleep deprivation have long been known to increase epileptic seizures.

I feel that a third necessary factor is focal brain injury related to trauma, infection, or toxic insult. The location of this injury determines the scope of the repetitive, stereotyped symptoms, which becomes the "reaction" kindled by the external stimulus whether chemical, electrical, and/or stress and sleep deprived related.

Conclusions

1. It appears that perhaps some of the mystery of chemical sensitivity syndrome is beginning to disappear. Repeated small exposures to inhaled toxins, chemical or visual kindling, auditory, and/or electrical stimulation, or single overwhelming exposures, acting on focal injuries can bring about sensitization of the brain's limbic system injury.

2. Because the brain's limbic system modulates emotions and memory organization systems, emotional and memory symptoms will be common features of the disease. This area of the brain also controls balance, gastrointestinal motility, the autonomic nervous system, and auditory and visual integration of stimuli as well as memory

3. Repeated exposures after the kindling or sensitization of the focus has occurred will produce effects out of proportion to the intensity of the exposure.

4 Cacosmic people seem more at risk than non-cacsomic people; but this has not yet been proved by a prospective study.

5. Stress may play some role in who becomes affected, but how big a role is still uncertain. Stress definitely increases the occurrence of "reactions", as does sleep deprivation due to its effect on focal brain irritability.

6. Because a fundamental brain mechanism is involved in the production of chemical sensitivity, continued exposure of individuals without protection or treatment is sure to increase the number of affected individuals and the severity of the symptoms in any particular individual.

TREATMENT

To be effective, treatment must interrupt these processes. Certainly avoidance of the stimuli can stop the setting off of the focal firing either directly or by stopping the kindling. Medications that stabilize the irritated cell decreasing its sensitivity to the kindling stimulus would be helpful. In this approach the amino acid anticonvulsant gabapentin has been very promising in our experience. Decreasing stress and improving sleep will also be beneficial. Removing any toxin that is still present in the brain should also decrease cell irritability. Desensitizations of all types, allergic, and behavioral, seem to provide benefit.

The charity Invest in ME has provided a truly remarkable opportunity to address one of the biggest medical scandals in history and to remove what in 2007 Alex Fergusson, Presiding Officer (Speaker) of the Scottish Parliament, referred to as "the cold grip of psychiatry" on myalgic encephalomyelitis (ME), which he said was "still far too deeply rooted in the world of ME"Now, however, despite the power and control of the psychiatric lobby, thanks to Invest in ME and the invaluable support of Jonathan Edwards, Emeritus Professor of Connective Tissue Medicine at University College, London, (world-renowned for his work in B cell immunology and as lead researcher in the clinical trials of rituximab for rheumatoid arthritis), the neuro-immune disease ME is at last about to enter the realm of mainstream medicine in the UK under the guidance of Professor Edwards himself.Invest in ME are at the forefront of international biomedical research and have by sheer determination and effort managed to put things in place for a trial of rituximab to begin on ME patients in the UK.They recognise the urgency of the situation and know that many ME patients do not have the luxury of time.

The charity already has the facilities in place, including suitably experienced researchers (Professor Jo Cambridge is now principal researcher at UCL, and the ME trial will involve the same team working under her that carried out the rituximab research in RA).The Clinical Trials Unit at UCL is already working on the protocol, and Invest in ME have agreed with Professor Edwards that the protocol will be externally reviewed even though the UCL team will make sure it is cast-iron by their own internal reviewers.

Invest in ME have been told this trial could start relatively quickly if the charity had funds available.

Such an opportunity must not be lost. However, this will not happen without substantial funding.

We therefore ask everyone who is able to do so to donate whatever they can afford, in order that the UK rituximab trial can get under way as quickly as possible whilst the excellent facilities and committed staff at UCL and the active support of Professor Edwards remain available, so that ME can finally be recognised as the devastating multi-system neuro-immune disease that it is and - most importantly -- so that sufferers may at last have some hope of alleviation of their suffering.Invest in ME have assured us that all donations to the rituximab fund will sit in a separate account which is totally ring-fenced, and should the trial not proceed, the following statement on the IiME website will be honoured:What Happens With These Funds If The Project Does Not Go Ahead:

If the rituximab project does not go ahead for some reason then the funds raised will be transferred to the IiME Biomedical Research Fund to fund other biomedical research projects which are attached to our proposal for an examination and research facility based in Norwich Research park in Norfolk, UK.

Q: You’ve been very aggressive about putting treatments forward for your patients. How many patients do you currently have on Ampligen, and how many have you treated with Ampligen in total?A: I have 28 people on Ampligen, with a total of 300. With respect to aggressive treatment, for severely disabled patients, and evenly the moderately disabled, unless you introduce some sort of aggressive treatment they don’t spontaneously recover. Symptomatic therapy can be enormously beneficial, but patients don’t recover unless you attack the etiology and pathogenesis directly. We’ve stumbled upon Ampligen, which is very beneficial for a subset of patients.

Q: Vistide (cidofovir) is one of the most difficult drugs to manage. What is your protocol?

A: I have a subset of patients who have evidence of beta herpesvirus reactivation, either CMV or HHV6a or b, and for that subset of patients, particularly if they have it in their spinal fluid, they need a very potent antiviral. For beta herpesviruses we are somewhat limited to a few oral drugs that are not terribly effective, to foscarnet, which is very difficult to administer, and Vistide which is somewhat easier because the infusion is every two weeks. I have treated 65 people according to this protocol, which, relative to the world of chronic fatigue syndrome, is not very many people. But some of those people have had very dramatic responses. Some have been able to go back to work, and to normal lives.

Q: Most doctors do not want to deal with Vistide, isn’t that true?

A: Vistide has to be monitored. You have to monitor kidney function, and liver function, and white blood cell count. I don’t even think it is generally acknowledged that [beta herpesvirus] subsets of these patients are identifiable.Q: Have you used Valcyte?A: I have used Valcyte. I follow the protocol of Jose Montoya at Stanford, with a long course of therapy. It also has to be monitored very carefully, and there are significant side effects such as headache and nausea, etc.

Q: Would you use it again now that you have Vistide?A: I still use it.

Q: From my personal experience [antivirals] do good for a while, then become ineffective. Is that universal?

A: With the herpesviruses, since we never really cure them, patients go into remission and then they relapse. This pattern also holds when patients are treated with Vistide. Most recently, I have been combining therapies, adding immunoglobulin, or Ampligen, or other agents, with some significant success.Q: What is the longest you have been able to keep a patient in good shape?

A: So far, three or four years, but I’m talking about almost total remission. I frequently get asked the question, “Is this curable?” I can’t say that it’s curable, but [the combination of therapies] is able to relieve symptoms so that people can return to work full time, which is pretty dramatic.

Q: Are you looking forward to CMX001 [a lipid antiviral used to boost the effectiveness of Vistide]?

A: Biopharma is great when they see a market, so I look forward to better drugs for all the patients with CFS, not just the subsets with immunological abnormalities. But they are not terribly interested, I think because they don’t recognize the market potential. They can’t get their hands on a biological marker and endpoints. All those things are very important when you are trying to interest pharma. And for a drug that’s already licensed there is no incentive for them to do a study.

Q: Are there any other immune boosters you are interested in?

A: IV gammaglobulin. A new area I’m excited about is the cytokine blockers and the immune modulator rituximab, which has gotten lot of press. Hopefully, they will do a much larger rituximab study in the near future. My concern with rituximab is that I don’t know how to predict who will respond. It would be nice to have guidelines, for entrance criteria, etc. where we could give people an idea of whether or not they will respond. The side effects can be very rough.

Q: If you had all the money in the world, in what direction would you be going now?

A: I would invest the money in centers for excellence. The reason is that primary care physicians can’t manage this disease. It’s too complex, too time-consuming, and they have too many other things to do. If we could get primary care physicians to recognize the disease, to qualify the patient, then they must have some place to refer them to. I see a great need all over the world for people to seek specialty care, which is appropriate until the disease becomes simpler to manage. HIV, for example, has become a very manageable disease. CFS /ME is a long ways from that.

Q: What do we need to do to get there?

A: I think it’s clear this is not a homogeneous disease. I think the CDC is correct in trying to understand subsets and redefine the subsets both biologically and by symptoms. Things would move along more quickly if we did that. As far as a universal definition is concerned, that would be enormously helpful, but we seem to have a great deal of difficulty getting there.Q: Do you see one or two subsets that predominate over the others?A: There seems to a real different between people who have an acute onset versus a gradual onset. About 15% of the people I see have active [viral] infections of one sort or another. They are clearly treatable and should be identified. There are people who have had industrial exposures or heavy metal toxicities, or post-vaccination, or post-transfusion onset. Those are all potentially identifiable subsets that might best be treated differently.Q: Why did chronic fatigue syndrome strike Lake Tahoe? Do you still have people coming in at a high rate?

A: Not locally. The local thing happened and disappeared. Some virus came through this community at that time, striking susceptible people, and then left. I mostly see people from distant places.Q: Who do you need to set up centers for excellence?A: The concept of translational medicine is very good, in which basic researchers work with clinicians – in this disease particularly, where there is not a lot of understanding between the scientists and the clinicians, or pharma for that matter. It would be doable because there are centers of excellence for breast cancer, for MS, for ALS, just go down the list. You can create that model if there is support for it.

Q: Wouldn’t major medical centers be a good place to start, like Stanford and Duke?A: Traditionally, major medical centers have been great sources for centers of excellence. However, they operate very slowly, and they have very high overhead. And funding has been very short term. Some people have started these plans and run out of funds.

Q: As a disease, we get most of our research funding from private funding. Is this an advantage over government funding?A: Private funding is very efficient. It can be targeted and it is easier to obtain in some circumstances. But this is a national problem that should be supported nationally. But I understand that with budget restrictions there is less and less available, particularly of these orphan diseases.Q: Couldn’t the same researchers who do research on MS, or lymphoma, or HIV, be doing research on CFS/ME with very little extra salary?A: That’s a hard sell. It goes back to the stigma of CFS/ME. The name just trivialized the disease. The lack of a clear-cut biological marker held off researchers, as well as short budget cycles, and low dollar amounts. A small grant gets you nowhere with this disease. You need large numbers of patients, which is why I totally support the OMI, with its idea of putting multiple physicians together, and adding all our patients. If you’re talking about things like genomic studies it takes a large number of patients in order to get a sufficient quantity for statistical validity. The same goes for treatment trials. With small treatment trials it’s very difficult to show efficacy.

Q: Is there any way to get researchers to focus on something other than blood? Lymph glands, for example?A: The Ian Lipkin studies at Columbia are looking at other tissues – saliva, urine, cerebrospinal fluid. I think he may be one of the first ones to do that. I am really excited about that research. Hopefully, he will help us in terms of biological markers, or pathogens, and possibly autoimmunity, and chemokine and cytokine signaling. I know he is working on all those avenues. We need people with his kind of expertise and quality to be researchers in this field.

Q: How have you stood it all these years, plugging along in spite of an utter lack of support?

A: That’s a question I get asked frequently. The best answer I can give is that there is still an essential truth that we have to find. Remember, I saw perfectly healthy people become disabled, and nothing can ever convince me that that was not a pathophysiological process. I expected the answer long before now, but I am still looking for answers. The second thing is that discovery comes to the prepared mind. We need intellectual curiosity. We need people asking questions about this, pursuing it. I haven’t seen the end of this story yet, and that’s why I am still in the field.

Web Seminar by Dr. Kenny De Meirleir, March 1, 2013Q: Oxygen Therapy: What Are the Pros and Cons?Administration of oxygen therapy has advantages and disadvantages. Oxygen increases the release of free radicals, which can be harmful. On the other hand oxygen can be very useful for people with severe pain and strong acidification. The oxygen used at home isn’t administered in oxygen cylinders any more. It comes from a device that transforms the air into almost 100% pure oxygen.

Q: Is the oxygen one gets in the hospital the same as your oxygen therapy?

The oxygen one gets from an oxygenator is the equivalent to the oxygen one gets in a hospital.Q: What do you expect from rituximab?

I don’t consider this to be a long-term solution, because practically all patients relapse. A new injection is necessary after six to twelve months, which is extremely expensive. The young and healthy B-cells formed after rituximab treatment will function properly in the beginning, but after a while they will again become involved in the disease process. Therefore rituximab isn’t a definitive solution.Q: Is Ampligen effective? For whom? How does it work?My experience with Ampligen dates from 1992-2001. We gave Ampligen to approximately 150 people during that time. Ampligen partially works like interferon and combats the viral aspect of the disease. So, those ME patients in whom the viral aspect of the disease is dominant will profit most from it.

Q: Are you familiar with fecal transplants? Is this a useful approach?We have heard of some patients who have chosen to have a stool transplant. During the transplant, stool from the intestines is removed and replaced by stool from a healthy individual. I believe this can also provide temporary improvement as fewer toxins are released in the body. But, again, it is not a definitive solution, because the problem isn’t so much the intestines as the immunity of the intestines. The abnormal flora will grow again. In addition, a stool transplant isn’t a pleasant experience, and must be repeated regularly. The only indication for this in ME patients is for those who have an overgrowth of C. difficile, which is extremely toxic, but the same would hold true even for people who don’t have ME.

Q: Can you briefly explain heart-rate monitoring and pacing? What do you expect from these?Several researchers have found that ME patients have irregular heart rhythms. This is due to changes in the sympathetic nervous system, causing inadequate control over heart rhythm. I do think that monitoring can help, but again, this isn’t a treatment of the cause. Pacing helps patients to use less energy. That is, energy is reserved for those things which are essential, in order to make it through the day. Pacing is an alternative for people who are chronically ill and who have few treatment options. They must learn to deal with the amount of energy they have left. Pacing should be addressed when the patient has tried all normal treatments.

Q: Doesn’t long-term administration of antibiotics kill the colonic flora?When one administers broad-spectrum antibiotics for a very long time, then one destroys the colonic flora. But when one is very careful and uses narrow-spectrum antibiotics to treat a specific infection this will not happen. There are numerous examples, as in tuberculosis, in which one administers antibiotics for eighteen months. But treatment involves a narrow-spectrum antibiotic, and therefore the colonic flora aren’t seriously disturbed. In the case of very acute infection one chooses broad-spectrum antibiotics. But when one is going to use long-term antibiotics to combat a very specific intracellular infection one chooses a narrow-spectrum antibiotic that has little effect on the colonic flora.

By Cort JohnsonFirst published onSimmaron Neuroimmune Research Foundation. April 9, 2013 “These results show objective endpoints, subset selection, and recovery. There were complete responders and partial responders among severely ill CFS patients with HHV6 or CMV. These are encouraging results for this subset and further well-designed trials should be pursued to confirm them.” Dr. Dan Peterson. At the HHV6 Conference in Paris, France today Dr. Peterson reported on the results of a retrospective study following 65 severely ill chronic fatigue syndrome patients given a course of Vistide from 2005-2012 for HHV6 and/or HCMV infections. Despite the interest in pathogens in ME/CFS, antiviral studies are rare and this is the first one reported for this drug. Vistide (Cidofovir) gets a lot less press than other antivirals and immunomodulators (Ampligen, Rituximab, Valcyte, Valtrex) used in this disorder probably because the drug requires a complex infusion protocol, frequent blood tests because of the rare but real possibility of serious kidney side effects, and is expensive (although it can be covered by insurance). This combination – infusions, frequent blood tests and expense – requires close physician follow-up. With Dr. Peterson’s specialized focus on patients with dysfunctional natural killer cells, however, he may be most consistent about testing for herpesviruses, which are known to be active in ME/CFS patients. After three decades of focusing on immunologically challenged ME/CFS patients, Peterson may be more experienced at pathogen detection and treatment than any other practitioner in the field, and so it’s not surprising to find the first Vistide study coming from his office. In an interview, a former patient of his said, ‘he leaves no stones unturned’; when he finds something he goes after it ‘aggressively’. In his presentation he stated almost 30% of his patients test positive for HHV-6 or human cytomegalovirus (HCMV) (PCR, rapid culture, antigenemia), and a whopping 50% test positive for Epstein-Barr virus (EBNA). Serious Drug For A Serious Illness Vistide (Cidofovir) is FDA approved for the treatment of cytomegalovirus (CMV) in patients with AIDS. (Cytomegalovirus is a member of the herpesvirus family.) and it’s been used off-label to treat human papillomavirus, BHK virus, herpes simplex virus, vaccinia virus infections. The Black Box warning on Vistide speaks for itself:"Cases of acute renal failure resulting in dialysis and/or contributing to death have occurred with few as one or two doses of Vistide. The “recommended dose, rate, frequency of Vistide injections must not be exceeded.” The Study A positive response was denoted by a negative pathogen test, improved fatigue and cognitive functioning determined by an interview with Dr. Peterson and the patient’s self reports after the trial. Response

Full Responders - Patients were deemed to be full responders if they were able to completely return to work or to work-related activities

Partial Responders – demonstrated significant improvement of symptoms but were unable to return to work or work related activities.

Non-Responders – Did not demonstrate any measurable improvement post-treatment

Results Dr. Peterson reported that seventy percent of patients were full (able to return to work) or partial (significant increase in functionality) responders; a very high rate of success in a illness characterized by a poor response to treatments. Only thirty percent of Vistide recipients did not have a significantly positive response to the drug. No serious side effects were seen; ironically the minor side effects seen were attributed to a drug, Probocenid, used to ensure Vistide was safe. It’s not clear what percentage of ME/CFS patients will test positive for HHV6 or cytomegalovirus in other practices but this type of response suggests the drug may be being under-used. With the FDA Stakeholder’s meeting coming up in three weeks and the Chronic Fatigue Initiative’s pathogen discovery study results due to be published later this year, Dr. Peterson’s presentation is timely. (Unfortunately, Dr. Peterson was not invited to present at the FDA Stakeholder’s Meeting.) Dr. Peterson called for placebo-controlled, double-blinded multi-center studies that address Vistide’s efficacy, examine its effects on the immune system and study the mechanisms of increase in VO2 max scores in ME/CFS. Sample Cases Dr. Peterson reported on several cases, all of whom were men – something Dr. Peterson has said he likes to do to break up the notion that only women get this disorder. A 27-year-old college graduate unable to work because of constant flu-like symptoms, weakness and marked cognitive decline (math!) presented with low NK functioning, low VO2 max and HHV6 and cytomegalovirus infection. He was able to return to work after 24 weeks of bi-weekly infusions. His VO2 max on the exercise test went up went up 23%, his NK cells a remarkable 400% and he tested negative for both viruses at the end of treatment. He had had ME/CFS for three years. A 54-year-old former high school teacher unable to work due to extreme fatigue, flu-like symptoms and cognitive problems severe enough to keep him from being able to grade his students papers presented with active HHV6 and cytomegalovirus infections and low NK cell functioning and VO2 max. He was able to return to work after 24 weeks of bi-weekly infusions. His VO2 max increased 47%, his NK function test went up 20% and he tested negative for both viruses. He had had ME/CFS for five years. The third patient had classic, acute onset ME/CFS which progressed to seizures. Both serum and cerebral spinal fluid tested positive for HHV6. At the end of the Cifodovir trial the viral load in his cerebral spinal fluid dropped from 3670 copies/ml to undetectable levels. Serum HHV6 was dramatically reduced (47,000 copies/ml to 3,000 copies/ml). Still symptomatic and experiencing cognitive problems, he was nonetheless able to return to work. Conclusions The retrospective study indicated Vistide (cifodovir) can have dramatic effects on functional capacity in HHV6 and/or HCMV infected ME/CFS patients. Increasing VO2 max appeared to be critical to increasing functionality as the partial responders did not increase their VO2 max while on Cifodovir. At the FDA Advisory Meeting for Ampligen Dr. Bateman noted that VO2 max test results probably were, given the exertional problems in ME/CFS, the most difficult to ‘move’ test result in this disorder. VO2 max levels in Dr. Peterson’s patients prior to Vistide administration were exceedingly low; they appeared to in the ‘very low’ range even for people for 65 years of age and older. Vistide moved those test results about 20% on average; leaving them still, it appeared, below normal but sufficient enough for a significant increase in functionality. A Vistide Example The VO2 max tests suggested most patients had not returned to full health and Dr. Peterson has said he knows of few complete recoveries. I interviewed a former patient of Dr. Peterson’s several years ago. Faced with the loss of his career and the ability to care financially for his family, Vistide turned out to be a godsend. Cut down by acute onset ME/CFS, his VO2 max score topped out at an unbelievably low 15 (which qualified him for heart disease) and he was a ’2′ out of 10 on his own energy scale (had trouble sitting up to eat). Within a month on Vistide he was at a ’4′; the next month he was a ’5′ and sleeping soundly for the first time since he’d gotten sick. The next month he was a ’7′ and his VO2 max tests had doubled to 28; still far below the 44 expected at his age, but an amazing increase, nevertheless. Three months later he was at ’90%’, back at work and able to do everything except exercise. CMX001 – The Future Vistide? Dr. Peterson didn’t report on CMX001 in Paris, but sitting in the background of all this is a analogue of Vistide called CMX001 which appears to be a safer and more effective, if not yet available, version of it. A 2012 review named CMX001 as one the ‘ten hot topics’ in antiviral research. Chimerix Pharmaceuticals modified Vistide so that it can easily be taken up into the tissues. That means no need for infusions, no worries about kidney problem and according to Chimerix, dramatically increased effectiveness. CMX001 has been in development for some time but just this March the FDA awarded the drug ‘fast track’ status for the prevention of cytomegalovirus infection. Phase II trials are finished and Phase III trials will get underway this year. Given Dr. Peterson’s success with Vistide, FDA approval of CMX001 could be very good news for ME/CFS patients with HHV6, HCMV and/or possibly EBV infections. Wrap Up In a retrospective study Vistide proved to be effective in treating severely ill ME/CFS patients with HHV6 and HCMV infections. Dr. Peterson called for double-blinded, placebo-controlled studies to further study Vistide’s efficacy and mechanism of effect. The CFI’s pathogen discovery studies due out this year should shed light on what percentage of ME/CFS patients could benefit from Vistide. A Vistide analogue under development called CMX001 which does not require infusions and does not effect the kidneys could be boon for ME/CFS patients with herpesvirus infections if it is approved by the FDA. CMX001 was given fast-track status by the FDA earlier this year.

For decades, a heated debate has raged over the nature of the illness known variously as chronic fatigue syndrome (CFS) and/or myalgic encephalomyelitis (ME). Historically, the two warring camps have been divided between “it’s all in their heads” and “we’re still looking.” But while both sides have consistently referred to CFS/ME as an “enigma,” it turns out the source of the illness may very well have been under everyone’s nose the whole time.

In the May 2013 issue of Discover Magazine, an article by Jill Neimark bearing the intriguing title, “Are B-Cells to Blame for Chronic Fatigue Syndrome?,” chronicled a remarkable discovery: wiping out the B-cells of patients with CFS/ME can actually cure the illness.

In 2007 Øystein Fluge and Olav Mella, two Norwegian oncologists at Haukeland University Hospital in Bergen, Norway, accidentally discovered that rituximab, a drug employed to treat Hodgkin’s lymphoma (as well as autoimmune disorders such as rheumatoid arthritis and Wegener's granulomatosis) cured several of their patients with CFS/ME. The news made instant headlines.

Inspired by their success, Fluge and Mella conducted a pilot study of rituximab on three patients with CFS/ME. The patients were given rituximab in an open-label trial (that is, the patients knew they were receiving the drug). All three patients experienced significant improvement; two of them responded within six weeks and the third had a delayed response, occurring six months after treatment. The positive effects lasted for between 16 and 44 weeks. After relapse, the patients were administered another dose of rituximab, with the same positive results. The investigators hypothesized that B-cells of the immune system might play a significant role in CFS, at least for a subset of patients, and that “CFS may be amenable to therapeutic interventions aimed at modifying B-cell number and function.”

The positive results of this, as well as a second open-label trial, led Drs. Fluge and Mella to conduct a larger study with a more rigorous design to test the effects of the drug. In 2009 they initiated a double-blind, placebo-controlled phase trial with 30 CFS/ME patients. As in the earlier open-label studies, the responses to rituximab were significant. Sustained overall improvements were noted in 67% of the patients (as opposed to 13% of the control group). Four of the rituximab patients showed improvement past the study period. The authors concluded that the delayed responses starting from 2–7 months after rituximab treatment, in spite of rapid B-cell depletion, “suggests that CFS is an autoimmune disease and may be consistent with the gradual elimination of autoantibodies preceding clinical responses.”

The unprecedented success of these small trials has led to a $2.1 million privately funded initiative spearheaded by the Norwegian nonprofit group, ME and You.

This is all very topical, but is it news? Dr. Paul Cheney, an immunologist, and one of the physicians who treated CFS/ME patients during the Incline Village outbreak, stated nearly thirty years ago that CFS/ME was the result of immune system upregulation. In fact, the prevailing theory during the 1980s and 1990s was that the immune systems of people with CFS simply did not shut off after the initial infection, but remained on “high.” This was considered the driving force behind CFS/ME, and, not coincidentally, is the basis for autoimmune disease.

Nonetheless, the idea that CFS/ME was an autoimmune disease languished for decades, even though the on-the-ground evidence has been apparent all along. The waxing and waning symptoms that are typical of CFS/ME are also typical of autoimmune diseases. Frequent comorbidities of CFS/ME with autoimmune diseases - e.g. Sjögren’s Syndrome and Hashimoto’s disease - were tip-offs that an autoimmune process was involved. And even if researchers didn’t care to take symptoms and comorbidity into account, there were dozens of studies documenting immune system abnormalities, particularly increased inflammatory cytokines, as well as a high incidence of markers such as antinuclear antibodies (ANA), and anti-cardiolipin antibodies (ACA), both of which are associated with autoimmunity.

The sad fact is that although the evidence was there, it was ignored. In a recent review of the accumulated evidence for autoimmunity in CFS/ME (in a chapter titled “Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Parallels with Autoimmune Disorders”) Ekua Brenu and associates site over 180 related articles. Their conclusion? "CFS/ME may have a potential to be described as autoimmune, as this is the only consistent immunological abnormality associated with CFS/ME.”

Given the thorough nature of the review, Brenu's conclusion, however cautious, was warranted. And, bearing out Brenu's review, as well as the rituximab studies, in March 2013 a UK study by Bradley et al found an increased number of naïve B-cells in patients with CFS/ME. An increase in naïve B-cells is a hallmark of autoimmune disease. In short, if it walks like a duck, and it quacks like a duck, it’s a duck.

Apropos of the rituximab studies, and as an excuse for not noticing the duck-like nature of CFS/ME, Neimark quotes rheumatologist Jonathan Edwards as saying, “T-cells were in fashion for a long time. B-cells were just considered boring.” It is hard to imagine that the absence of research on fully half of the immune system could be due to the whims of fashion, but whimsy is only part of the explanation for this exercise in mass denial. The other component is that the major players in our health care system - government agencies, researchers, physicians, insurance companies – have had a vested interest in perpetuating the myth that CFS/ME is an unknown and unknowable entity.

Norwegians, apparently, have less invested in the myth. When the results of Fluge and Mella’s rituximab study were made public, the Norwegian Directorate of Health Deputy Director Bjørn Guldvog was prompted to issue a televised apology. "I think that we have not cared for people with ME to a great enough extent,” he said. “I think it is correct to say that we have not established proper health care services for these people, and I regret that."

Originally posted on Herb Wisdom as "Health Benefits of Bee Propolis." By C.L. Davis The benefits of bee propolis have been well-known for a long time but, as with many natural remedies, some of this knowledge has been obscured in recent times. Using natural substances to cure various ailments is something that our ancestors did with much success. Many people are now re-discovering the benefits of using natural remedies, such as propolis. About Bee PropolisHoneybees collect more than just pollen when they are buzzing around the yard. Resins are collected from various plants and trees, mixed with beeswax and amino acids and used to form structures within the hive, similar to the way that we use cement. Bees need to protect themselves from disease just like we do and propolis is their solution. As the bees travel through the hive, they rub against the propolis and receive the benefits of the natural antibiotic, anti-inflammatory, antifungal and antiviral properties from their building materials. Active Ingredients & Uses Immune BoostPropolis has antibiotic and anti-microbial properties. Because propolis is high in the vitamin B complex vitamins, has significant amounts of vitamin C, and contains vitamin E, it naturally boosts the immune system. High levels of antioxidants are also found in propolis and these also give our natural immune system functions a boost, as well as doing the same for the bees! Because of its ability to enhance the function of the immune system, Propolis is a great treatment for cold and flu symptoms and even food poisioning. It can be taken in the form of capsules or as a tincture and is easy to obtain. Wound HealingBee propolis also promotes wound healing, making it very useful in topical treatments such as ointments and creams. It is easy for burns, abrasions and lacerations to become infected, but when treated with a strong antibacterial agent the body has a chance to heal quickly and with less chance of scarring. Studies conducted in several different countries show that bee propolis has strong antibacterial and anti-microbial properties. As an anti-inflammatory, bee propolis has been shown to be very effective. This is another way in which propolis can be useful as a topical treatment for wounds. Anti-InflammatoryTaken internally, it can also reduce the damaging effects of inflammation in the body. Inflammation is the cause of many diseases, including heart disease, inflammatory bowel disease, some bone diseases, pelvic inflammatory disease and arthritis. Autoimmune diseases such as endometriosis have also been shown to respond well to treatments that include the use of propolis. Anti-ViralThe anti-viral property of bee propolis is another one of its well-known benefits. Viruses such as herpes can cause painful and embarrassing canker sores but relief has been found by using bee propolis. It can be taken internally to inhibit the action of the virus and used topically to treat blisters and canker sores. The antiviral properties of bee propolis are also what make it so effective in treating colds and the flu. Warts, which are thought to be caused by viruses or deficiencies in the immune system, have also been treated successfully with propolis. Allergy ReliefRats were shown to produce less histamine when given propolis, indicating that it has the potential to be effective in providing allergy relief. Anti-FungalPropolis’ antifungal property is another one of its benefits. Common fungal infections include yeast infections of the mouth and vagina, foot fungus and jock-itch. Propolis has been shown to be an effective antifungal agent in a variety of studies. It can be used in the form of a topical treatment, as a tincture or in capsule form. Its effectiveness is due in part to enhancement of the immune system, and in part to its natural antifungal properties. Cancer & Chemotherapy ReliefIn some studies, propolis has also been shown to be effective against cancer cells. Propolis was applied as a tincture to cancerous prostate and colon cells, among others and caused significant rates of cancer cell death. Healthy cells were not destroyed, which is what happens in chemotherapy. Studies of the benefits of propolis in treating cancer are ongoing, but show that there is a possibility that some of the devastating effects of chemotherapy could be reduced by making use of bee propolis. How To UseBee propolis is available in a number of forms, such as ointments, lotions, tinctures and capsules. It can be used to heal burns and other wounds, clear up infections, reduce the impact of inflammatory diseases and fight viruses. Some studies have even indicated that bee propolis can be used to treat cancer. Its antibiotic, anti-inflammatory, antifungal and antiviral properties have been known to humankind for ages and proven effective in numerous scientific studies the world over.

Research from Queen Mary, University of London suggests that omega-3 fatty acids, which are found in fish oil, have the potential to protect nerves from injury and help them to regenerate.

When nerves are damaged because of an accident or injury, patients experience pain, weakness and muscle paralysis which can leave them disabled, and recovery rates are poor.

The study, published in Janurary, 2012 in the Journal of Neuroscience, suggests that omega-3 fatty acids could play a significant role in speeding recovery from nerve injury.

The study focused on peripheral nerve cells. Peripheral nerves are the nerves which transmit signals between the brain and spinal cord, and the rest of the body.

These nerves have the ability to regenerate but, despite advances in surgical techniques, patients usually only have good recovery when their injury is minor.Omega-3 fatty acids are vital for the body’s normal growth and development and have been widely researched for their health benefits. Because the body cannot manufacture omega-3 fatty acids, they have to be consumed in foods such as oily fish.

In the new study, researchers first looked at isolated mouse nerve cells. They simulated the type of damage caused by accident or injury, by either stretching the cells or starving them of oxygen. Both types of damage killed a significant number of nerve cells but enrichment with omega-3 fatty acids in cells gave them significant protection and decreased cell death.

Next the researchers studied the sciatic nerves of mice. They found that a high level of omega-3 fatty acids helped mice to recover from sciatic nerve injury more quickly and more fully, and that their muscles were less likely to waste following nerve damage.

The research was carried out by a group led by Adina Michael-Titus, Professor of Neuroscience at Barts and The London Medical School and lead of the Neurotrauma and Neurodegeneration group in the Centre for Neuroscience and Trauma, Queen Mary, University of London.

She explained: “Our previous research has shown that these fatty acids could have beneficial effects in a number of neurological conditions. This new study suggests that they could also have a role in treating peripheral nerve injuries.“More work is needed but our research indicates that omega-3 fatty acids can protect damaged nerve cells, which is a critical first step in a successful neurological recovery.”

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About me:I'm a 25-year veteran of CFIDS. I know what it is like to be bedbound for long stretches of time. I also know what it is like to recover, and to relapse. But this blog is not about my personal experience. It is intended to be a resource - a collection of anything that might be helpful to the CFIDS community: book reviews, advice, CFIDS news, research, advocacy, opinion, who's who in our community, fundraising... and occasionally a bit of humor.

Disclaimer: I am not a doctor, which means nothing I write, no matter how sensible it may be, should be interpreted as medical advice.